Trypanosoma musculi infections of mice are typified by phases of: Rapid growth of the parasites in the blood and peritoneal space (PS); "plateau"; and, after about 2 wk, rapid immune elimination and cure. During the course of infection immune responses are markedly inhibited. Initiation of immune elimination of the parasites coincides with the release from inhibition. We know little about: (a) immune processes that effect parasite elimination; (b) mechanisms responsible for the prolonged inhibition of immunity; or (c) events underlying the termination of inhibition and recovery of immune responses. We do know that there is variation among inbred mice in susceptibility to T. musculi and, especially, that aged animals suffer much more severe infections than young-adults. The murine/T. musculi infections; and (b) the causes of age-related deterioration of those processes. Major candidates for the immune processes are antibody (Ab)-dependent cytotoxicity (ADCC) and Ab-promoted hepatic phagocytosis. The component of these processes likely to suffer most from parasite-induced inhibition and age-related debilitation is the elaboration of humoral antibodies. We will study young and aged mice, of a susceptible and resistant strain, with respect to: (a) the quantity and quality of parasite-specific antibodies generated during infections; (b) the types and competence of ADCC effector cells and (c) the efficiency of hepatic clearance. Clones of T. musculi and a panel of monoclonal antibodies (at hand) will aid the investigation. The restriction of interleukin 2 availability by the combined effects of aging and parasite infection will be explored. Suppressor cells will be studied. This research will reveal much about the nature of the deterioration of immune processes that expose the aged individual to infections.